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NUR 326 > Dysrhythmias > Flashcards

Dysrhythmias Flashcards

1
Q

functions of cardiac cells

A

automaticity
excitability
conductivity
contractility

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2
Q

what is automaticity

A

ability to generate electrical impulse

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3
Q

what is excitability

A

ability of a cell to respond to an outside stimulus
- chemical, mechanical, electrical

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4
Q

what is conductivity

A

ability to receive an electrical impulse and conduct it

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5
Q

what is contractility

A

ability of the myocardial cells to shorten in response to an impulse

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6
Q

what is depolarization

A

when the muscles squeeze
- contractions in the atria and ventricles
- during systole

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7
Q

what is repolarization

A

when the heart is preparing to contract again

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8
Q

what is the p wave

A

the first little bump
- atria squeeze/depolarize

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9
Q

what is the QRS complex

A

the big jump
- ventricle squeezes/depolarize
- atria repolarize and get blocked by this

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10
Q

what is the t wave

A

the small bump after the QRS
- ventricles repolarize

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11
Q

what initiates the p wave

A

SA node

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12
Q

what initiates the QRS complex

A

AV node

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13
Q

how does the AV node know when to go

A

senses the depolarization of the atria

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14
Q

what are function of the bundle of HIS and purkinje fibers

A

responsible for telling ventricles to squeeze

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15
Q

normal electrical conductivity of the heart is called

A

sinus rhythm

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16
Q

what are the characteristics of sinus rhythm

A

60-100
regular
P waves are upright, rounds, before q QRS, regular
PR interval: 0.12-0.20 sec
QRS: less than 0.12 sec

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17
Q

what is the amount of time a little box represents on an EKG

A

0.04 secs

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18
Q

what is sinus arrhythmia

A

another normal commonly seen in young ppl
- degree of variability
- HR fluctuates with respiration or autonomic nervous system (longer p to p intervals)
- no changes of cardiac output

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19
Q

what is a dysrhythmia

A

abnormality of the cardiac rhythm
- problems w impulse generation or conduction
- significant bc it affects cardiac output

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20
Q

what are causes of dysrhythmias

A

inappropriate automaticity
triggered activity
re entry

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21
Q

what is inappropriate automaticity

A

a cell that initiates APs when its not suppose to
- can appear in the atria
- ex: myocardial ischemia, electrolyte imbalance

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22
Q

what is triggered activity

A

an extra impulse generate during just after repolarization
- ex: digoxin toxicity, SNS stimulation, genetics

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23
Q

what is re entry

A

cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
- myocardial ischemia, electrolyte imbalance

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24
Q

what is sinus bradycardia

A

regular, less than 60, normal rhythm/PR interval/QRS
- originates in the SA node

25
Q

what are the causes of bradycardia

A

hyperkalemia
vagal response (vagus is stimulated)
digoxin toxicity
LATE hypoxia (low o2 for long time)
medications (beta block, ca channel block)
myocardial infarction (ischemia around SA node)

26
Q

what are the clinical manifestations of sinus bradycardia

A

lightheaded and dizzy
fatigue
syncope (fainting)
dyspnea
chest pain/discomfort
confusion

27
Q

why do clinical manifestation of sinus bradycardia occur

A

there is a dec of cardiac output

28
Q

when do we treat sinus bradycardia

A

when the patient has symptoms

29
Q

how do we treat bradycardia

A

atropine
pacemaker if drugs dont work

30
Q

what is sinus tachycardia

A

100-150, reg rhythm
P waves are typically normal and present but can be partially hidden
normal PR and QRS interval
* more common than brady *

31
Q

what are the causes of sinus tachycardia

A

catecholamines: exercise, pain, strong emotions
fever (inc metabolic rate)
FVD ( often first sign of dehydration)
medications (epi, albuterol)
substances (caffeine, cocaine, crack)
early hypoxia

32
Q

treatment for sinus tachycardia

A

depends on cause
- hypovolemia: fluids
- fever: antipyretics
- pain: analgesics
- beta blockers to reduce HR and myocardial oxygen consumption

33
Q

what is paroxysmal supraventricular tachycardia (PSVT)

A

occasional above the ventricle fast heart
- 150-250
- originates in the AV node
- usually no P wave and if present they are abnormal
- QRS normal
- caused by re entry phenomena
- begins and ends suddenly
- “heart is racing”

34
Q

PVST causes

A

over exertion
emotional stress
stimulants
digitalis toxicity
rheumatic heart disease
CAD
wolff parkinson white
RS HF

35
Q

PSVT clinical manifestations

A

palpations
chest pain
fatigue
lightheadedness or dizziness
dyspnea

36
Q

what happens to cardiac output with PSVT

A

dec CO bc heart cant squeeze enough volume with each beat and the heart will eventually get exhausted

37
Q

what are premature atrial contractions (PACs)

A

early p waves that usually have a morphologic change
- normal PR interval, QRS
- usually no consequences but if frequent can indicate potential other problems like afib

38
Q

what do you do for someone with premature atrial contractions

A

check electrolytes
may need O2

39
Q

what are the atrial dysrhythmias

A

atrial flutter
atrial fibrillation

40
Q

what is atrial flutter

A

originates in the AV node and overrides the SA node
- re entry impulse that is repetitive and cyclic
- reg atrial rhythm, but rate over 250
- ventricle rate is slower

41
Q

what happens to the waves in atrial flutter

A

P wave: sawtooth
QRS normal
maybe 2-4 p waves for 1 QRS (2:1, 3:1, etc)

42
Q

causes of atrial flutter

A

coronary heart disease
cardiomyopathy
heart valve disease
congenital heart disease
inflammation of the heart like myocarditis
HTN
conditions like lung disease of overactive thyroid
electrolytes

43
Q

what is atrial fibrillation

A

multiple irritable spots in the atria
- irregularly irregular (both atrial and ventricular –> not communicating and are going at random)
- 100-175
- no identifiable p wave –> fibrillation waves
- PR interval irregular?

44
Q

what are a fib clinical manifestations

A

palpations
heart racing
fatigue
dizziness
chest discomfort
SOB
may be symptomatic

45
Q

what are a fib causes

A

electrolytes
hypoxia
cardiovascular disease

46
Q

what are a fib complications

A

dec cardiac output
heart failure
embolus –> stroke
- blood not clearing out of atria, allows it to clot then can be pumped into circulation

47
Q

treatment of a fib

A

rate control: beat blockers, CCB, digitalis, amiodarone,
stroke prevention: anticoags, antiplatelets
non pharm: ablation, caridoversion

48
Q

what is premature ventricle contractions (PVCs)

A

contractions coming from ectopic focus in the ventricles
- comes earlier than QRS should come and doesnt allow for a normal p wave
- wide/distorted QRS

49
Q

what are the causes of PVCs

A

stimulants
electrolytes!!
hypoxia
fever
exercise
emotional stress
CVD

50
Q

how do we treat PVCs

A

treat the cause

51
Q

what are the PVCs subtypes and what are they

A

bi, tri, and quadrigeminy
- QRS distorted after
– q p wave
– q 2 p waves
– q 3 p waves

52
Q

what is ventricular tachycardia

A

3 or more PVCs together
- ventricles take control and fire repeatedly and no atrial contractions are occurring
seriously dec CO

53
Q

what is vtach associated with

A

MI
CAD
sign electrolyte imbalance
heart failure
drug toxicity

54
Q

what is the rate during vtach

A

150-200, reg

55
Q

what do the waves look like with vtach

A

no evident p waves
PR no measurable

56
Q

how do we treat vtach

A

depend on the pulse, pt will be asymptomatic very quick unless converts back to other rhythm
- anti dysrhythmic meds like beta blockers, Ca channel blockers
- electrolyte replacement

57
Q

first question to ask during vtach

A

pulse or pulseless
- pulseless = CPR

58
Q

what is ventricular fibrillation (vfib)

A

irregular waveforms of varying shapes and sizes
ventricles are just quivering
no effective contractions = no CO

NUR 326 (20 decks)

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